A 49-year-old male with a past medical history significant for male sexual encounters, gonorrhea, depression and prior negative HIV and syphilis screening presented to the Emergency Department sent by his PCP with abnormal lab results that included a RPR 1:32 and positive Treponema pallidum antibodies. The patient complained of subjective fevers for two weeks and one week of unsteady ‘intoxicated’ swaying gait that acutely worsened five days prior to arrival necessitating a cane. Recent admission and evaluation in an outside hospital resulted in a discharge diagnosis of vertigo after a normal head CT and laboratory examination.
The admitting physical exam revealed dysmetria, dysdiadochokinesia, ataxic gait and positive Romberg. MRA showed luminal irregularity and signal attenuation involving anterior circulation, bilaterally, potentially secondary to neurosyphilis vasculitis. Initial laboratory evaluation revealed RPR 1:16 and Penicillin G IV therapy was started from admission secondary to clinical picture and RPR positivity. This was met with skepticism from our neurology and ID consultants. Subsequently, lumbar puncture analysis resulted with reactive pleocytosis, occasional plasma cells, elevated protein, VDRL-CSF non-reactive, followed by reactive CSF FTA-ABS. New contextual findings included a positive HIV rapid antibody, RNA 1270 copies/mL and CD4 of 313 units/L. The patient’s ataxic gait rapidly improved. The patient was also evaluated for other possible etiologies including viral and autoimmune that were all negative.
Discussion:
Sir William Osler once said he who knows syphilis, knows medicine, while this is not true today, the concept that neurosyphilis (NS) is the “great mimicker,” making it difficult to recognize clinically is probably more true today. In the era of overuse of antibiotics and HIV co-infection, NS presentations are increasingly variable. Clinical suspicion and CSF examination are key to diagnosis. A reactive CSF-VDRL establishes the diagnosis; a non-reactive test does not exclude it and can be negative in up to 70% of patients. In contrast, CSF FTA-ABS (fluorescent treponemal antibody absorption) test is sensitive but not specific.
Conclusions:
Our patient’s atypical symptoms were attributed on prior evaluation at an outside hospital to vertigo and discordance within our health care team to include neurology and infectious disease resonated with skepticism for NS as the cause. The current recommendation is that patients who are HIV positive with suspected NS undergo various combinations of reactive serologic and CSF testing. Due to the underlying sensitivity and specificity profile for CSF VDRL, CSF FTA-ABS was pursued and captured the underlying diagnosis that historically and currently can be overlooked.